Lipids最新文献

Metabolic dysfunction-associated steatotic liver disease (MASLD) and valproic acid (VPA)-induced hepatotoxicity both involve dysregulated lipid metabolism. However, the specific effects of VPA on lipid metabolism in the context of MASLD remain unclear. This study aimed to investigate alterations in the lipid profile following VPA treatment using an oleic acid (OA)-induced cellular model of MASLD. After VPA treatment, non-targeted lipidomic analysis was performed. The results showed that VPA exacerbated lipid dysregulation by significantly increasing triglyceride (TAG) levels and promoting the accumulation of long-chain free fatty acids (FFAs) with carbon chain lengths between C20 and C26 in steatotic hepatocytes. Additionally, a positive correlation was observed between elevated TAG levels and the length of TAG carbon chains in VPA-treated steatotic hepatocytes. Disruptions in the homeostasis of phosphatidylethanolamines (PEs), lysophosphatidylethanolamines (LPEs), phosphatidylinositols (PIs), and sphingomyelins (SMs) were also observed. These findings indicate that VPA exacerbates lipid accumulation in steatotic hepatocytes, clarifying its role in worsening MASLD and highlighting the importance of risk–benefit assessment and hepatic monitoring in clinical management.

Dietary polyunsaturated fatty acids (PUFA), including conjugated linolenic acids, are increasingly investigated for their potential health benefits. Zebrafish have emerged as a promising in vivo model for studying the metabolism and effects of such bioactive compounds. The present study tested whether zebrafish tissues could be enriched with specific PUFA through dietary modulation. To do so, six-month-old female zebrafish were divided into four groups and fed purified diets over an eight-week period, each diet containing a distinct lipid source: sunflower oil (rich in linoleic acid), linseed oil (rich in alpha-linolenic acid), fish oil (rich in eicosapentaenoic acid and docosahexaenoic acid), and pomegranate seed oil (rich in punicic acid, a conjugated linolenic acid). Body mass, length, and whole-body fatty acid profile were then assessed. An efficient incorporation of linoleic acid, alpha-linolenic acid, eicosapentaenoic acid, docosahexaenoic acid, or punicic acid into zebrafish tissues was observed, depending on the dietary source. Linoleic acid and alpha-linolenic acid underwent partial bioconversion into longer and more unsaturated fatty acids. Fish fed with pomegranate seed oil were enriched in conjugated linoleic acids (rumenic acid and 18:2 (trans-9, trans-11)), suggesting the presence of a Δ13 reductase activity in zebrafish. These findings highlight the suitability of zebrafish as an in vivo model for investigating the impacts of specific dietary and metabolically derived PUFA in the context of health and disease.

We investigated molecular characteristics and tissue distribution of elongation of very long chain fatty acids (ELOVL) genes in the chicken (Gallus gallus) genome. The research specifically examines the expression levels of these genes in chickens fed diets enriched with varying concentrations of curcumin. The aim is to uncover the potential roles and functions of ELOVL genes in the metabolism of fatty acids (FAs) in this species. In the experimental design, Hy-Line Brown commercial laying hens were selected for a feeding trial lasting 10 weeks. During this period, the hens were fed diets supplemented with curcumin at 100, 200, 300, and 400 mg/kg. The results revealed several critical insights: (1) It was confirmed that the ELOVL genes in Gallus gallus are orthologues of those found in vertebrates, indicating a shared evolutionary lineage; (2) There were noteworthy differences in how ELOVL genes, except ELOVL1 and ELOVL7, were distributed across various tissues and how they responded to dietary curcumin, prompting the need for comprehensive promoter analyses to better understand their functions in chickens; (3) The addition of curcumin to the diet did not increase omega-3 FAs in egg yolk; and (4) Dietary curcumin modulated ELOVL mRNA transcription in Gallus gallus. However, the intricate and multifaceted nature of FA metabolism presents challenges to fully grasping the implications of these results, highlighting the necessity for further in-depth investigations in this area.

Dyslipidemia is a known risk factor for cardiovascular diseases (CVD). Research indicates that curcuminoids plus piperine co-supplementation (Curc + Pipe) can alter serum lipids. However, the findings from various studies are inconsistent. This meta-analysis aims to evaluate the efficacy of Curc + Pipe in serum lipid parameters in adults. A systematic search was conducted in databases until August 2025 to identify eligible randomized controlled trials (RCTs). To estimate the pooled effect size, weighted mean differences (WMDs) with corresponding 95% confidence intervals (CIs) were calculated, applying a random-effects model to account for potential variability between studies. A pooled analysis of 16 RCTs, encompassing a total of 1038 participants (Intervention: 522, Control: 516) revealed that Curc + Pipe significantly reduced triglycerides (TG) (WMD: −18.64 mg/mL, 95% CI: −29.94, −7.34, p < 0.001) and total cholesterol (TC) (WMD: −6.58 mg/mL, 95% CI: −12.60, −0.55, p = 0.032) and increased high-density lipoprotein cholesterol (HDL-C) (WMD: 1.51 mg/mL, 95% CI: 0.29, 2.72, p = 0.015). However, the reduction in low-density lipoprotein cholesterol (LDL-C) was not statistically significant (WMD: −2.20 mg/mL, 95% CI: −7.22, 2.80, p = 0.387). Curc + Pipe has clinically meaningful lipid-modulating effects, particularly in reducing TG and TC and modestly increasing HDL-C levels. These benefits were most pronounced in more prolonged supplementation in individuals with dyslipidemia, metabolic disorders, and overweight. Clinically, Curc + Pipe may serve as a valuable complementary therapy for dyslipidemia management to decrease the risk of CVD.

Attention has recently been paid to the cross-talk between G protein-coupled receptor 55 for lysophosphatidylinositol as an endogenous agonist and cannabinoid receptors 1 and 2 for 2-arachidonoylglycerol as an endogenous agonists in mammalian neuronal cells. In relation to the functional coupling, in this study, exogenously added 1-arachidonoyl lysophosphatidylinositol (1–20:4 LPI) to MG6, a mouse microglial cell line, was found to be converted to 1-arachidonoyl glycerol (1–20:4 MAG) and arachidonic acid (20:4 FFA), possibly due to the combined action of ecto-lysophospholipaase C activity of glycerophosphodiesterase 3 and extracellular lipase toward MAG. Consistent with the above result, exogenous 1–20:4 MAG was found to be converted to 20:4 FFA by extracellular lipase activity toward MAG in the culture medium of MG6 cells. Not only was exogenous 20:4 FFA incubated with MG6 cells, but also 20:4 FFA produced from the exogenous 1–20:4 MAG and 1–20:4 LPI in the absence of fetal bovine serum, respectively, were postulated to be involved in the reduced population of process-bearing MG6 cells via its entry into the cells and the intracellular conversion of prostaglandins. This hypothesis was supported by our findings showing that the reducing effects of exogenous 1–20:4 LPI, 1–20:4 MAG, and 20:4 FFA were all found to be indomethacin-inhibitable, and that exogenous PGD₂, but not PGE₂ and PGF₂α, was shown to reduce the population of process-bearing MG6 cells cultured without Fetal bovine serum.